Current investigations deal with the elucidation of the mechanism(s) by which complement activation at a cell surface stimulates prostaglandin synthesis with resultant bone resorption as determined by in vitro studies employing bones maintained in organ culture. This pathological process can be initiated by immunoglobulins which possess a specificity for cell surface antigens. Activation of either the classical or alternative complement pathway stimulates prostaglandin synthesis and bone resorption. The sequence of events culminating in bone destruction is currently being examined in terms of: 1) the mode of complement triggering of prostaglandin synthesis and the cells responsible for its production, 2) the interaction of the various cellular elements of bone which may play in this process, and 3) the direct effects of prostaglandins on the various cell types which may produce the ultimate destructive effects on bone.